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28 June 2010

This is an addition for archival purposes of a post that originally appeared at Scienceblogs.

In the winter of 1999, I stood in an outpatient clinic in a pediatric hospital in New Delhi and listened to a father sobbing over the paralysis of his only son. He was a farmer and lived in Uttar Pradesh; counting walks, minibuses and trains, it had taken him 24 hours to get to the hospital. He had carried the toddler the entire way.

His son had gotten the drops, he insisted: Every time the teams came to his neighborhood -- which they did three, four times each year -- he or his wife had lined up all their children, the boy and his older sisters. His son had had 11, 12 doses, the man said. How could he have gotten polio? And it was polio, the doctor treating him confirmed, not one of the transient febrile paralyses that exist alongside the disease and make detection and diagnosis so complex in resource-poor settings. She saw this all the time, she confided. The massive polio-eradication campaigns that continually blanketed India had trouble reaching some resistant populations, and those children contracted polio because they were not vaccinated -- but children whose parents were compliant, who believed in the drops and made sure their children received them, became paralyzed as well.

I was in India that winter because the long-hoped-for goal of the worldwide eradication of polio was supposed to be achieved the following year, in 2000. The global eradication initiative -- led by the WHO, the CDC and a massive volunteer effort by Rotary International -- didn't make that goal that year. Or in 2002, or in 2005. For a variety of reasons, from the biology of the disease in the tropics to political manipulation in service of unrelated ends, several countries have remained stubborn hot spots. And as long as the disease persists within their borders, it can leak outside them and become re-established in any area where vaccination has slowed down because the goal of stopping local transmission appears to have been achieved.

Most recently, it has leaked to Tajikistan, a country that has been polio-free since 2002 but shares borders with three of the four countries -- India, Pakistan and Afghanistan (Nigeria is the fourth) -- where polio remains endemic. As of the last count, 183 children were confirmed to have polio; authorities generally estimate that for every child detected with polio, 200 others may be infected silently and can pass on the disease.

There is so much to say about polio eradication; it is an impossibly complex and expensive task, fraught with cultural complexities and burdened with an endgame of clean-up that will stretch years beyond eradication itself. It is so complex that major public health figures have periodically thrown up their hands and declared eradication unachievable. It is one of the most expensive public health campaigns every attempted, with billions spent so far (and yet chronically short of funds). And because most of the West remains fully vaccinated, polio lurks far below the radar horizon of our concern.

I say all this -- which is kind of opening the floodgates for me, because I've wanted to talk about polio for years, but it is a damn hard story to sell to editors -- because CMAJ, the Canadian Medical Association Journal, has published a great editorial calling for the West to take the threat of polio seriously again.

Although the rates of poliovirus immunization in most of Europe exceed 90%, neither the Ukraine nor Georgia has reached this target. Furthermore, regions of Canada and some European countries have very low rates of vaccine uptake. Infants and toddlers are often not vaccinated on time because of a lack of appreciation of the seriousness of poliomyelitis. Community immunization rates may also be adversely influenced by concerns about vaccine safety, religious beliefs barring vaccination and antivaccine or antigovernment sentiments... There are no cures for poliomyelitis -- prevention through vaccination is our best and only defence. We are only one asymptomatic infected traveller away from an outbreak because of low vaccination rates. (MacDonald and Hebert)

Since the year 2000, there have been two recurrences of polio in the US: one in Minnesota, sparked by the vaccine virus, and one in Arizona contracted by a college student traveling abroad. The college student, and the children in the Minnesota community, had never been vaccinated because of religious or cultural exemptions. So our protections are not as impermeable as we think.

24 June 2010

This is an addition for archival purposes of a post that originally appeared at Scienceblogs.

There's a troubling item in this afternoon's issue of the CDC's Morbidity and Mortality Weekly Report or MMWR: The first report in the United States of a novel resistance mechanism that renders gram-negative bacteria extremely drug-resistant and that has been linked to medical care carried out in India or Pakistan.

The short item describes three isolates (E. coli, Klebsiella pneumoniae and Enterobacter cloacae) found in three patients in three states between January and June of this year. All three isolates produced New Delhi metallo-beta-lactamase (NDM-1), which has never been recorded in the US before. Because of that novel mechanism, the three isolates were resistant to the carbapenems usually used on the most serious gram-negative infections, in fact to all beta-lactam antibiotics (penicillins, cephalosporins, carbapenems, monobactams, etc.) except for one monobactam, aztreonam -- and they were also resistant to aztreonam through another mechanism that hasn't been identified yet. All three of the patients found carrying this novel resistance factor had undergone medical care in South Asia recently.

This may be the first finding of this mechanism in the US, but it's been causing alarm in Europe for at least two years.

The first identification of NDM-1 was in 2008, in a 59-year-old resident of Sweden who was of South Asian origin and had returned to India for several months. The man was not well -- he had long-standing type 2 diabetes and had experienced a number of strokes -- and while in India he was hospitalized for an abscess, underwent surgery, developed bedsores and was treated for them as well. He returned to Sweden and was hospitalized there in January 2008, where physicians found him to be suffering from a urinary tract infection caused by a Klebsiella strain carrying this never-seen resistance mechanism.

Last July, the UK's Health Protection Agency put out a national alert about NDM-1, warning that the novel mechanism had gone from never-seen in 2007, to 4 isolates in 2008, to 18 in the first half of 2009. They were not an outbreak, but represented repeated importations: The isolates were clonally diverse and had been collected at 17 different hospitals. They were, instead, a sign that long-standing two-way population movement between England and South Asia -- augmented by elective medical tourism (two patients had gone to India for cosmetic surgery) -- was bringing the high rates of antibiotic resistance in India back to a UK medical system that is already challenged by serious infection-control problems.

And now it's here. The special challenge of NDM-1 (which as today's finding suggests is on a mobile genetic element that has carried the resistance mechanism between species) is not only that it adds to an accumulatingrogues' galleryof resistance factors that are rapidly making gram-negative bacteria ferociously drug-resistant, but also that there are so few drugs under development for gram-negatives that truly untreatable infections are not far off. The UK clearly is already struggling with attempting to use drugs that are old and toxic, untested against these organisms (and therefore with no agreed-upon dosing), or wrong for the organ systems affected:

Treatment presents major challenges. Most isolates with NDM-1 enzyme are resistant to all standard intravenous antibiotics for treatment of severe infections. Polymyxin is usually active in vitro ... but of uncertain clinical efficacy, especially in pneumonia, owing to poor lung penetration. Tigecycline is often active in vitro, but has low serum levels, is unsuitable for urinary infections and, more generally, is of unproven efficacy in severe infections.

The CDC's alert today asks any clinicians who come up against carbapenem-resistant gram-negatives to ask about contact with India or Pakistan as part of history-taking, and to forward isolates through state public health labs to the the CDC.

Update + fodder: I flipped over to my RSS reader and also discovered this paper posted overnight by Clinical Infectious Diseases, about extended-spectrum beta-lactamases in a particular strain of E. coli ("an important new public health threat"), and this one in Emerging Infectious Diseases, about carbapenem resistance moving between Klebsiella and E. coli.

17 June 2010

This is an addition for archival purposes of a post that originally appeared at Scienceblogs.

A set of papers published this month in two journals provide an unsettling glimpse into the rocketing incidence and complex epidemiology of one really scary pathogen, Acinetobacter baumanii.

In the all-star annals of resistant bugs, A. baumanii is an underappreciated player. If people -- other than, you know, disease geeks -- recognize it, that is because it's become known in the past few years for its propensity to attack wounded veterans shipped to military hospitals from Iraq and Afghanistan, earning it the nickname "Iraqibacter." (Important note: Steve Silberman of Wired magazine took an early look at this phenomenon in 2007, in a great story that analyzed the epidemiology of Iraqibacter to show that military infection control, not the environment of Iraq, was to blame for the bug's rapid emergence.) A. baumanii is a nasty bug, causing not just wound infections but pneumonia, urinary tract infections, meningitis and bacteremia. Even more nasty, it collects resistance factors like baseball cards, and is commonly resistant to at least 4 antibiotic classes. The most resistant strains are susceptible only to the so-toxic-we-put-it-back-on-the-shelf-decades-ago antibiotic colistin.

This is a particular concern because A. baumanii is a Gram-negative bacterium -- and while the drug-development pipeline for Gram-positives such as MRSA has slowed practically to a trickle, the one for Gram-negatives has dripped itself dry. As the Infectious Diseases Society of America and Jerome Groopman of the New Yorker highlighted back in 2008, drugs for Gram-negatives are barely on the agenda for the few companies still conducting antibiotic development.

So, the first piece of bad news. In Infection Control and Hospital Epidemiology (ICHE), a team from Brooke Army Medical Center in San Antonio take a look at their incidence of resistant Ab and find it exploding. Between 2001 and 2008, the percentage of A. baumanii isolates that were resistant to at least 3 classes of drugs went from 4% to 55%; of all the isolates, 17% (127) were resistant to at least 4 drug classes, and one was resistant to, well, everything.

How does A. baumanii spread so fast? A second paper in ICHE suggests a reason: The bug seems to do a better job than other resistant pathogens of contaminating the gear and hands of health care workers. A study done at University of Maryland found that when health care workers took care of A. baumanii patients, they ended up with contaminated gowns and gloves 39% of the time, and with contaminated hands (after glove removal) 4.5% of the time. Those are higher rates than for MRSA (18.5% of encounters) or VRE (8.5%).

A review article in Clinical Infectious Diseases reminds us why we should care about this: It examines the drugs to which some strains of A. baumanii are still susceptible, and finds all of them significantly toxic to different organs (kidneys, liver, pancreas, red blood cells, ) at the doses necessary to wipe out the bug.

Which is all troubling by itself. But a paper and editorial also appearing in Clinical Infectious Diseases make the case for A. baumanii as a bigger threat than has been understood. The bug's recent epidemiology has shown a distinct split, between the highly resistant forms affecting veterans, most of them being treated in the military evacuation chain, and less-resistant forms affecting civilians in hospitals (including in the Brooks data in the paper above). The severe wounds, aggressive treatment and rapid multiple transfers of personnel in the military system inadvertently created an environment that not only put A. baumanii under great selective pressure, but also spread it with startling efficiency.

The paper, reporting data from 4 community hospitals near Detroit, shows that the civilian medical system -- that would be the one that most of us live in -- has duplicated that churning as well. Between 2003 and 2008, all A. baumanii in their network increased 25%. A. baumanii resistant to the first 2 front-line drugs went from 2% to 33% of isolates. And "pan-resistant" A. baumanii -- resistant to all 8 drugs available for it, an essentially untreatable strain -- went from nonexistent to 14% of all the isolates that network found.

The effect on the patients was dramatic, of course: The more resistant their strains were, the more likely they were to never go home from the hospital, but (if they did not die there) to be discharged instead to a nursing home, long-term acute care facility, or hospice. But the larger point is that they carried that multiply-resistant strain with them, distributing it throughout the region: Patients came to those 4 hospitals, carrying A. baumanii, from 17 different nursing homes; from the 4 hospitals, carrying A. baumanii, they were transferred out to 28 different nursing homes.

This is a smart analysis, and devastating in its implications. American hospitals do a debatable job right now of handling infection control -- but overwhelmingly, they are handling infection control as individual institutions, not as competitors in a local market, and certainly not as members of a geographic region. Yet this data demonstrates clearly that cooperation between hospitals and other healthcare institutions -- most of which don't have hospitals' infection-control budgets or personnel -- is going to be essential if we want to put the brakes on Acinetobacter before it soars in the civilian medical system in the same way it did in the military one.

15 June 2010

This is an addition for archival purposes of a post that originally appeared at Scienceblogs.

The Center for Global Development, a DC think-tank, is releasing what looks like a thoughtful report aimed at refocusing policy debates over drug resistance toward the epidemic's global impact, with particular attention to the the developing world.

From the report's preface:

Problems with drug resistance have moved from the patient's bedside to threaten global public health. Drug resistance has dramatically increased the costs of fighting tuberculosis (TB) and malaria, has slowed gains against childhood dysentery and pneumonia, and threatens to undermine the push to treat people living with HIV/AIDS effectively. Global health funders and development agencies have cause to worry about whether their investments in access to drugs, and global health programming more broadly, are being undone by the relentless advance of drug resistance.

It calls out a sustained lack of leadership:

Past efforts to energize global action to more comprehensively address drug resistance have been sidetracked by poor timing or over-stretched budgets... In an unfortunate coincidence of timing, a WHO Strategy on Antimicrobial Resistance was launched on September 11, 2001. As a result, the action plan prepared for the Strategy did not get carried out, and over time the interest in cross-cutting drug resistance at WHO withered, even while disease-specific attention grew. For many years, the U.S. Government provided support for research, technical support, surveillance, and policy development on drug resistance in developing countries through an annual budget appropriation to the U.S. Agency for International Development (USAID). That support has become narrowed to programming in only a few areas.

It recommends 4 specific steps:

Improve surveillance by collecting and sharing resistance information across networks of laboratories

This is an addition for archival purposes of a post that originally appeared at Scienceblogs

Via the Journal of the American Medical Association, a report from Spain: the first recorded outbreak, in a Madrid hospital, of Staphylococcus aureus resistant to linezolid (Zyvox), one of only a few drugs still available to treat very serious infections of drug-resistant staph, MRSA. This is bad news.

Background: The M in MRSA stands for methicillin, the first of the semi-synthetic penicillins, created by Beecham Laboratories in 1960 in response to a worldwide 1950s outbreak of penicillin-resistant staph. The central feature of the chemical structure of both penicillin and methicillin is an arrangement of four atoms, known as the beta-lactam ring, that governs both drugs' ability to interfere with bacterial cell-wall synthesis. That structure was copied into the formulas of a number of other drug families -- the cephalosporins, carbapenems and monobactams -- and so MRSA is resistant to them as well. And in addition, the bug has picked up resistance to yet other drug families through horizontal transfer; so increasing the census of new drugs that can treat resistant staph infections is a high priority for drug development. It's especially critical for severe infections such as ventilator-associated pneumonia, osteomyelitis, endocarditis and bacteremia, since all the remaining last-resort drugs have challenges from toxicities to ineffectiveness in certain organs.

Linezolid is a relatively new drug, out since 2000 (and, as a downside, still under patent and, according to patients who have been prescribed it, very expensive). It was the first of a new drug class, the oxazolidinones; since there were no "me too" similarities to older drugs, clinicians hoped that resistance to linezolid would be slow in coming.

No such luck.

The first recognized case of linezolid resistance in staph was recorded in 2001. Still, there have been relatively few cases of LRSA, or staph that possesses both linezolid and beta-lactam resistance: 8 cases in the US to date, 2 in Germany and 1 each in Brazil, Colombia and the UK.They have all been caused by a particular point mutation, G2576T.

This Spanish outbreak, though, had a different cause, the importation of the cfr gene, which also mediates resistance to the older drugs clindamycin and chloramphenicol, apparently on a plasmid, possibly from a staph strain common in cows. The outbreak caused by this new mechanism was as large as the entire known burden of LRSA to date: 12 patients, over 10 weeks in 2008, in 3 linked ICUs, pls 3 patients who were not in intensive care, but had had previous ICU stays. Six of the patients had ventilator-associated pneumonia and 3 were bacteremic. Six died -- though the authors are careful to say that all of these patients were critically ill, with brain tumor and esophageal cancer among other problems, and that LRSA was not directly responsible for all of the deaths.

More bad news: There were actually 4 clones of LRSA within this outbreak, with slightly different resistance patterns. Troublingly, one of the 4 had reduced sensitivity to glycopeptides; the chief glycopeptide is vancomycin, which has been the go-to drug for MRSA for 50 years.

The hospital checked its staff and the ICU environments, and found nothing of significance; there was no reservoir in the hospital that was passing this newly resistant strain to patients. With no obvious solution there, they dialed back sharply on their linezolid use, going from more than 200 doses per day in April 2008 to 25 doses per day in June. That aggressive antibiotic stewardship appears to have put the brakes on the outbreak, and after June, no additional cases were recorded.

An accompanying editorial underlines how critical antibiotic stewardship was in controlling this outbreak, while also pointing out how very liberal the hospital was in prescribing linezolid before the outbreak began -- suggesting that if the institution had used its antibiotics more conservatively from the start, this outbreak might not have arisen, or at least not have been as large.

No one doubts the importance of infection-control practices in limiting outbreaks with antibiotic-resistant organisms, but optimizing antibiotic use remains essential for successful control of such outbreaks...No longer can clinicians' unrestricted use of antibiotics and ignoring suggestions from those who attempt to improve or alter antibiotic use be tolerated. Clinicians must understand the sense of urgency about the appropriate use of antibiotics.

10 June 2010

This is an addition for archival purposes of a post that originally appeared at Scienceblogs

A couple of days ago, I talked about the link between a potentially massive hepatitis B outbreak in West Virginia and the lack of access to primary dental care. I was mushyqualitatively descriptive, ahem, about the number of people who lack access to dental insurance.

Comes now the CDC to save the day. In a statistical brief posted today, the National Center for Health Statistics gives a concise but thorough overview of the state of dental insurance in the US. Short version: Ain't pretty.

172 million non-elderly Americans have private health insurance. (NB, leaving 46 million non-elderly with no health insurance, which matches the usually accepted figures.)

Of them, 45 million have no dental coverage -- which, added to the 46 million with no insurance at all, means that more than 90 million Americans have no dental coverage at all. (I believe the technical term for a number that large is a crapton. Maybe a metric crapton.)

In addition:

If you have employer-provided health insurance, your chances of having dental coverage are pretty good: 80%.

If you have privately purchased insurance of any kind, not so much: 30%.

So, reinforcing Monday's point: There are multiple millions of Americans who get no assistance paying for dental care, which is a largely cash-only business. (And judging from my own experience -- thanks to my childhood in the UK, I have teeth like chalk and consume more than my share of dental care -- dental insurance negotiates discounts. So self-pay dental care is relatively more costly.) And therefore, it is not surprising that thousands of people attended that free dental clinic in northeastern West Virginia, and were potentially exposed to hepatitis B as a result.

08 June 2010

This is an addition for archival purposes of a post that originally appeared at Scienceblogs.

The Subcommittee on Health of the Energy and Commerce Committee of the House of Representatives has announced a hearing for Wednesday: "Promoting the Development of Antibiotics and Ensuring Judicious Use in Humans."

Sandra Fryhofer, M.D., Council on Science and Public Health, American Medical Association

John S. Bradley, M.D., American Academy of Pediatrics, Chief, Division of Infectious Diseases, Department of Pediatrics, University of California, San Diego, School of Medicine, Clinical Director, Division of Infectious Diseases, Rady Children's Hospital

This is the second hearing the Health Subcommittee has had this spring, apparently at the prompting of the chairman of Energy and Commerce, Rep. Henry Waxman, who made the opening statement at the first such hearing in April:

We need to debate the health care bill and review its implementation. But we ought to be able to chew gum and walk at the same time. Because it is not going to make much difference if you have health insurance or not if you are going to die from something that could have been prevented from an antibiotic. And we are seeing more and more antibiotic resistance. (Transcript)

Reading between the lines, I'm going to guess this hearing will lean heavily on the IDSA's campaign to improve market conditions for pharma companies in order to revive antibiotic development (an issue I discussed recently at the old Superbug -- we're working on getting the archives moved over).

07 June 2010

Constant readers, I have an exciting announcement. After 3 years here on Blogger, SUPERBUG has been invited to join the thoughtful, knowledgeable, chatty and sometimes raucous community over at Scienceblogs. From today, I'll be posting instead at a new page:http://scienceblogs.com/superbug.

I will keep this site up as a resource, at least until we can work out the mechanics of transferring this blog's archives over to the new page.

You've been such great readers, so thoughtful and thorough. I really hope you'll follow me over to the new location. I would love to engage with you there too.

Sincere thanks to all of you for all your attention, and warmest wishes.

This is an addition for archival purposes of a post that originally appeared at Scienceblogs.

Via ProMED Mail comes a news report that about 2,000 people in 5 states are being sought by health departments so they can be checked for hepatitis B infection. The potential source: the Mission of Mercy Dental Clinic, a free dental-care fair held just about a year ago in Berkeley County in the far north-east corner of West Virginia. The potentially infected include 1,137 people who were treated at the two-day clinic and 826 of the volunteers who worked there, from West Virginia, Washington, D.C., Virginia, Maryland, Pennsylvania and North Carolina. Three patients and two volunteers have already been diagnosed. The virus in four of the five matched on molecular fingerprinting, suggesting a common source; the fifth patient refused further testing.

Hepatitis B is blood-borne, so on the surface, this is a story of the tragic consequences of some failure somewhere in the clinic's infection-control procedures. (One reason why it caught my eye, since I'm interested in healthcare-associated infections.) Except that it's not -- or not only. It's important to unpick why such an extraordinarily large number of people may have been exposed at one time. Looked at through that lens, it becomes a story about what can happen when we don't fund basic health care in a timely way.

Some background: West Virginia is one of the poorest states in the country and has some of the highest rates of the usually recognized diseases of poverty: tobacco use, chronic kidney disease, asthma, cardiovascular disease. (Look for West Virginia on these CDC maps of incidence of heart disease and stroke.) But it also has extraordinarily high rates of another health problem that ought to be linked in the public mind to low socioeconomic status, but usually isn't: untreated dental disease. Eric Eyre of the Charleston Gazette (disclosure: a friend and fellow Kaiser Foundation Fellow) took a year-long close look at dental disease in the state in 2006-07 (slideshow, stories). If you're squeamish, I advise skipping the one about the woman yanking her own teeth with pliers after a few shots of moonshine.

Dental disease -- that's not just cavities, but tooth loss, bone loss, abscess, Ludwig's angina, septicemia in the most serious cases -- isn't only a problem for West Virginia, though it happens to be worst there. It's a problem all over the US because, without ever intending to, we've allowed dental care to become a primarily cash-based form of medicine.

If you have a job, you may have dental insurance, though it's a less-common employment benefit than health insurance, and covers comparatively less of the cost of any procedure. If you don't have a job, dental care is entirely out of pocket. If you're poor enough to be on Medicaid, whether or not you have dental coverage depends on which state you live in, because Medicaid dental coverage for adults falls under the portion of Medicaid funded by the states, not the federal government. In the past 12 months, California, Hawaii, Massachusetts, Michigan, Minnesota, North Carolina, and Washington state all cut or tried to cut their contributions to dental Medicaid from their state budgets. If you're the child of a poor family, you are hypothetically entitled to Medicaid-funded dental care, though that depends on being able to find a local dentist willing to accept Medicaid reimbursement; last year, the Government Accountability Office said that children have trouble finding Medicaid-accepting dentists in 43 out of 50 states.

Net result: Untreated dental disease is now the most common disease of childhood, five times more common than asthma according to a 2000 Surgeon General's report, and emergency room visits for dental crises are rising steadily. ERs are not the right place to treat dental problems -- they don't fill cavities or do extractions, though they can drain abscesses and give antibiotics and pain meds -- but as with so much else in US medicine, ERs offer a mandated clinic of last resort when there's nowhere else to go. (For more about the interplay between dental care and ER overcrowding, here's a story I wrote for the June Annals of Emergency Medicine.)

All of that explains why thousands of people from a wide swath of the East Coast were so desperate for free dental care that they were willing to stand in line overnight in a high school parking lot. (The first free dental clinic in West Virginia had to close its doors early after it got 1,100 patients in the first 2 hours.) And also why hundreds of dental-care professionals and students and community volunteers were so eager to help. And why they're all now waiting by the mailbox, wondering whether they're in line for a letter that will tell them where to get tested for infection with a life-long chronic disease.

04 June 2010

Some of you may have spotted an announcement last week from the Centers for Disease Control and Prevention about a release of data from the National Healthcare Safety Network (NHSN), a repository of hospital infection data. You can guess the big news in the report from its title, "First State-Specific Healthcare-Associated Infections Summary Data Report": For the first time, database users are able to calculate healthcare-associated infections (let's call them HAIs for short) by state, as well as nationally.

Good news, you would think. And it is. According to the CDC's announcement (press release, press conference transcript), the national rate of one particular type of HAIs, central line associated bloodstream infections or CLABSIs (like it looks — pronounced "klab-sees") is down 18% from the previous 3 years. Taken together, all HAIs kill at least 100,000 Americans each year (an old number that is probably an underestimate) and cost at least $30 billion per year. CLABSIs are an important component of the spectrum of HAIs and may account for a third of all HAI deaths — so any reduction is a positive development.

And yet: The bigger news about this report, unfortunately, is that it lays bare how little we really know about HAIs, and how little progress has been made in preventing or even documenting them.

Consider:

The report includes data from only 17 states

The data does not match state to state, so state rates cannot be compared

Participation in the NHSN by hospitals is voluntary (except in states that recently have passed mandatory reporting laws) and data is self-reported

Hospitals that report to the NHSN are not identified (in fact, unless state laws say otherwise, they are guaranteed anonymity)

The NHSN does not collect data on the most problematic HAI organisms, MRSA and C. difficile.

If you think for a moment about how incomplete this data is, and how much the data collection allows hospitals to avoid saying, then Dr. Peter Pronovost's remarks to the Association of Health Care Journalists in April begin to make sense. Pronovost is a MacArthur Fellow for his championship of evidence-based infection prevention, and said (sorry, no verbatim record that I know of, but I live-tweeted his speech) that if hospital infection reporting were truly transparent and truly accountable — right now, it's neither — the problem of HAIs would end tomorrow, because consumers would be so shocked that they would rise up and demand change.

The CDC says there will be additional data and a new comparison with this first snapshot within about 6 months. Again, that's all good news. But it's worth taking a deep look at this report to really understand how little we know — which will also help to explain why this problem so persistently fails to get better.

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Maryn McKenna is an award-winning journalist and author and a recovering newspaper reporter. She writes about public health, medicine and food policy for national magazines and medical journals, and finds emerging diseases strangely exciting.

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SUPERBUG has been featured on Fresh Air with Terry Gross, NPR's Science Friday, CBC's The Current and other radio and TV as well as numerous print and online publications. Find it at Superbugthebook.com.